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Abstract
Respiratory viral infections trigger asthma exacerbations, yet the acute effects of Toll-like receptor 7 (TLR7) signaling on airway physiology are poorly understood. This study shows that TLR7 agonists rapidly abolish airway smooth muscle contraction in guinea pigs, mice, and humans. Bronchodilation occurs via TLR7-dependent nitric oxide pathways and TLR7-independent mechanisms involving prostaglandins and potassium channels. Reduced efficacy in allergen-sensitized and virus-infected models suggests a link to asthma severity and TLR7 polymorphisms. Despite diminished potency, TLR7 agonists retain bronchodilatory activity, indicating potential as a combined prophylactic and rescue therapy for asthma, offering a novel approach to reduce medication burden and side effects.